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LECT2 functions as a hepatokine that links obesity to skeletal muscle insulin resistance

フォーマット:
論文
責任表示:
Lan, Fei ; Misu, Hirofumi ; Chikamoto, Keita ; Takayama, Hiroaki ; Kikuchi, Akihiro ; Mohri, Kensuke ; Takata, Noboru ; Hayashi, Hiroto ; Matsuzawa-Nagata, Naoto ; Takeshita, Yumie ; Noda, Hiroyo ; Matsumoto, Yukako ; Ota, Tsuguhito ; Nagano, Toru ; Nakagen, Masatoshi ; Miyamoto, Ken-ichi ; Takatsuki, Kanako ; Seo, Toru ; Iwayama, Kaito ; Tokuyama, Kunpei ; Matsugo, Seiichi ; Tang, Hong ; Saito, Yoshiro ; Yamagoe, Satoshi ; Kaneko, Shuichi ; Takamura, Toshinari
言語:
英語
出版情報:
American Diabetes Association, 2014-05-01
著者名:
Lan, Fei
Misu, Hirofumi
Chikamoto, Keita
Takayama, Hiroaki
Kikuchi, Akihiro
Mohri, Kensuke
Takata, Noboru
Hayashi, Hiroto
Matsuzawa-Nagata, Naoto
Takeshita, Yumie
Noda, Hiroyo
Matsumoto, Yukako
Ota, Tsuguhito
Nagano, Toru
Nakagen, Masatoshi
Miyamoto, Ken-ichi
Takatsuki, Kanako
Seo, Toru
Iwayama, Kaito
Tokuyama, Kunpei
Matsugo, Seiichi
Tang, Hong
Saito, Yoshiro
Yamagoe, Satoshi
Kaneko, Shuichi
Takamura, Toshinari
続きを見る
掲載情報:
Diabetes
ISSN:
1939-327x  CiNii Research  Webcat Plus  JAIRO
巻:
63
通号:
5
開始ページ:
1649
終了ページ:
1664
バージョン:
author
概要:
Recent articles have reported an association between fatty liver disease and systemic insulin resistance in humans, but the causal relationship remains unclear. The liver may contribute to muscle insulin resistance by releasing secretory proteins called hepatokines. Here we demonstrate that leukocyte cell-derived chemotaxin 2 (LECT2), an energy-sensing hepatokine, is a link between obesity and skeletal muscle insulin resistance. Circulating LECT2 positively correlated with the severity of both obesity and insulin resistance in humans. LECT2 expression was negatively regulated by starvation-sensing kinase adenosine monophosphate-activated protein kinase in H4IIEC hepatocytes. Genetic deletion of LECT2 in mice increased insulin sensitivity in the skeletal muscle. Treatment with recombinant LECT2 protein impaired insulin signaling via phosphorylation of Jun NH2-terminal kinase in C2C12 myocytes. These results demonstrate the involvement of LECT2 in glucose metabolism and suggest that LECT2 may be a therapeutic target for obesity-associated insulin resistance. © 2014 by the American Diabetes Association. 続きを見る
URL:
http://hdl.handle.net/2297/37595
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